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Article

Plastin 3 is upregulated in iPSC-derived motoneurons from asymptomatic SMN1-deleted individuals.

Cellular and molecular life sciences : CMLS - 1 May 2016

Heesen Ludwig, Peitz Michael, Torres-Benito Laura, Hölker Irmgard, Hupperich Kristina, Dobrindt Kristina, Jungverdorben Johannes, Ritzenhofen Swetlana, Weykopf Beatrice, Eckert Daniela, Hosseini-Barkooie Seyyed Mohsen, Storbeck Markus, Fusaki Noemi, Lonigro Renata, Heller Raoul, Kye Min Jeong, Brüstle Oliver, Wirth Brunhilde

Abstract excerpt

Spinal muscular atrophy (SMA) is a devastating motoneuron (MN) disorder caused by homozygous loss of SMN1. Rarely, SMN1-deleted individuals are fully asymptomatic despite carrying identical SMN2 copies as their SMA III-affected siblings suggesting protection by genetic modifiers other than SMN2. High plastin 3 (PLS3) expression has previously been found in lymphoblastoid cells but not in fibroblasts of...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 26573968
DOI: 10.1007/s00018-015-2084-y
PMCID: PMC11108513

Genes

PLS3
SMN1
SMN2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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